In attempting to construct a neuropsychology of anxiety, findings
can be drawn from several related, yet often perceived as separate, domains of research, including cognitive science and neuroscience. The relatively new fields of cognitive neuroscience and
affective neuroscience are concerned with very similar questions
regarding brain-behaviour relationships as were fundamental to
the older field of neuropsychology, and the neuroimaging tools
central to those disciplines are no less pertinent to neuropsychology than are traditional neuropsychological test batteries or
cognitive/behavioural paradigms. Thus, this review of the neuropsychological findings in anxiety disorders covers a wide array
of methods that together inform knowledge of the brain mechanisms involved in the circuitry governing pathological forms of
anxiety.

Although often overlooked by neuroscientists studying brain
function in anxiety, cognitive research over the past two decades
has contributed substantially to knowledge about brain function in
anxiety. A large body of work demonstrates that anxiety disorders are characterized by cognitive biases, indicating a heightened
response to the possibility of threat (for review, see McNally, 1998).
Attentional biases have been elicited very reliably across a variety
of paradigms in which potentially threatening information is associated with greater attentional capture in individuals with anxiety
disorders than in controls. The interference of this attentional capture with other cognitive processing serves as the operationalization
of this bias in research studies. Furthermore, attentional biases have
been found to disappear upon remission (for review, see McNally,
1998), suggesting that such biases are state-dependent. Cognitive
biases have also been observed in the form of interpretation and
memory biases. Across a number of different paradigms involving
ambiguous stimuli that can be interpreted as threatening or neutral,
anxious people choose the threatening meaning. Accruing evidence
suggests that anxiety disorders are also accompanied by enhanced
memory for negative or threatening information under certain conditions. These cognitive data suggest dysfunctional activation of a
right hemisphere system involved in threat perception (for review,
see Nitschke, Heller and Miller, 2000; see also Compton et al.,
2000, 2002).

In addition to these cognitive biases, cognitive deficits have been
documented in anxiety disorders. One is a tendency to do poorly on
tasks that require selective attention and concentration. This deficit
has been suggested to reflect a general problem of preoccupation
and distraction due to worry or rumination that interferes with
other mental processes (for review, see Nitschke, Heller and Miller,
2000). Compromised visual-spatial functioning has also been
reported. In addition, individuals with posttraumatic stress disorder
often exhibit deficits in explicit memory. Taken together, these
cognitive deficits suggest aberrant frontal, anterior cingulate, right
parietal, and hippocampal functioning. Building on this cognitive
research as well as on behavioural and electroencephalographic
(EEG) findings (for review, see Nitschke, Heller and Miller, 2000)
and an extensive literature in non-human animals examining fear
and anxiety (for reviews, see LeDoux, 1996; Davis and Lee, 1998),
haemodynamic neuroimaging research has implicated a number of
the suggested regions.

Although emotional, cognitive, and neural commonalities are
apparent, the diversity of findings also warrants the importance
of respecting unique patterns and heterogeneity both among and
within the various anxiety disorders. An observation that has
become increasingly salient in the burgeoning neuropsychological
literature on anxiety and its disorders is the lack of clarity
and specificity about what anxiety is. Views of anxiety range
from its usage in contemporary clinical research as a rubric
term that encompasses fear, panic, worry, and all the anxiety
disorders listed in the DSM-IV to its very specific operationalization
referring to context conditioning and long-term sensitization (e.g.,
Davis and Lee, 1998) to a more generic personality dimension
closely linked to neuroticism (e.g., Gray, 1982). Further, the
heterogeneity within each of the different anxiety disorders has
become increasingly apparent and represents a major problem for
investigators attempting to uncover the neurobiological correlates of
individual anxiety disorders. Inconsistencies across studies may be
explained by the fact that anxiety is not a unitary phenomenon and
that different types and symptoms of anxiety are associated with
particular cognitive patterns (Heller and Nitschke, 1998; Nitschke,
Heller and Miller, 2000). An important mission of neuroscience
research in this area is to help unravel the inchoate notions of
anxiety that currently exist. Thus, although it is important to look
for generalizations regarding the neural mechanisms of anxiety, it is
also necessary to consider the possibility of heterogeneity by being
as specific as possible regarding the disorder or type of anxiety
under investigation.

The aim of this chapter is to assess what is known about the
neuropsychology and neural circuitry of anxiety disorders by examining the relevant cognitive research. Structural and functional
neuroimaging data will also be reviewed, including morphometric magnetic resonance imaging (MRI), functional MRI (fMRI),
positron emission tomography (PET) using various radiotracers
such as [18F]fluorodeoxyglucose (FDG) for glucose metabolism
and 15O-labelled water for blood flow, single-photon emission
computed tomography (SPECT) with l33Xenon or 99mTc-HMPAO,
and scalp-recorded EEG. This review of the cognitive and neuroscience literatures reveals that the anxiety disorders engage
brain regions involved in threat perception (e.g., right hemisphere

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